Foxtail millet downy mildew, caused by the obligate parasite Sclerospora graminicola, is a highly devastating disease for foxtail millet. S. graminicola infection often damages buds, leaves, and spikes, significantly compromising its quality and yield. However, resistant varieties can effectively reduce susceptibility to pathogen attacks. In this study, we investigated Jingu21 (JG21) and the resistant mutant rdm12, which was generated by ethyl methanesulfonate (EMS) mutagenesis. Phenotypic observations showed that rdm12 did not differ significantly from JG21 in agronomic and quality traits. Notably, rdm12 exhibited enhanced disease resistance, along with increased activities of defense enzymes and higher levels of osmoregulatory substances. Transcriptome analysis of rdm12 mutants and JG21 revealed that differentially expressed genes (DEGs) were mainly enriched in pathways such as plant-pathogen interaction, MAPK signaling, diterpenoid biosynthesis, and glutathione metabolism. The differential expression of several key genes—including receptor protein kinase genes, WRKY transcription factors, pathogenesis-related (PR) proteins, calmodulin, glutathione S-transferase—contributed to improved downy mildew resistance in the mutants. In particular, WRKY transcription factor 53 (encoded by Seita.3G139400), pathogenesis-related protein PRMS (encoded by Seita.3G175100), and G-type lectin S-receptor-like serine/threonine protein kinase (encoded by Seita.7G095600) played an essential role in resistance during S. graminicola infection. This study identifies key genes and important products involved in resistance, along with their associated metabolic pathways, thereby elucidating the resistance mechanism of foxtail millet against S. graminicola. These findings provide a theoretical foundation for resistance screening in foxtail millet.
Han et al. (2026) studied this question.